Product Name	BRMS1
Chinese Name	乳腺癌转移抑制基因1抗体
Alias	Breast cancer metastasis suppressor 1; Breast cancer metastasis-suppressor 1; BRMS-1; BRMS1_HUMAN; DKFZp564A063; MGC95128; AV003220; AW554636.
Research Area	Tumour  immunology  Epigenetics
Immunogen Species	Rabbit
Clonality	Polyclonal
React Species	Human, Mouse, Rat,  (predicted: Dog, Pig, Horse, )
Applications	WB=1:500-2000 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500 （Paraffin sections need antigen repair） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
Theoretical molecular weight	28kDa
Cellular localization	The nucleus cytoplasmic
Form	Liquid
Concentration	1mg/ml
immunogen	KLH conjugated synthetic peptide derived from human BRMS1: 151-246/246
Lsotype	IgG
Purification	affinity purified by Protein A
Buffer Solution	0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage	Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
Attention	This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed	PubMed
Product Detail	Breast cancer metastasis-suppressor 1 (BRMS1) is 246 amino acid protein that acts as a mediator of metastasis suppression in several types of cancer including ovarian, lung, bladder, and murine mammary. BRMS1 mRNA is expressed in various tissues, including ovary, prostate, testis, and colon, but the protein is primarily detected in term placenta. BRMS1 suppresses metastasis without inhibiting tumorigenicity by modifying several metastasis-associated phenotypes. BRMS1 may participate in transcriptional regulation by binding to the mSin3/histone deacetylase complex. The expression of BRMS1 in certain cells increases connexin Cx43 expression and reduces connexin Cx32 expression. This produces a gap junction that increases intercellular communication, similar to those found in normal breast tissue. BRMS1 is stabilized by Hsp90 and may inhibit NF-ⅹB activity. Function: Transcriptional repressor. Down-regulates transcription activation by NF-kappa-B by promoting the deacetylation of RELA at 'Lys-310'. Promotes HDAC1 binding to promoter regions. Down-regulates expression of anti-apoptotic genes that are controlled by NF-kappa-B. Promotes apoptosis in cells that have inadequate adherence to a substrate, a process called anoikis, and may thereby inhibit metastasis. May be a mediator of metastasis suppression in breast carcinoma. Subunit: Belongs to the BRMS1 family. Subcellular Location: Nucleus. Cytoplasm. Predominantly nuclear. Tissue Specificity: Expression levels are higher in term placentas than in early placentas. Low levels of expression observed in normal pregnancies and in molar pregnancies. Similarity: Belongs to the BRMS1 family. SWISS: Q9HCU9 Gene ID: 25855 Database links: Entrez Gene: 25855 Human Omim: 606259 Human SwissProt: Q9HCU9 Human Unigene: 100426 Human
Product Picture	Sample: HepG2(Human) Cell Lysate at 30 ug Primary: Anti-BRMS1 (SL8686R) at 1/1000 dilution Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution Predicted band size: 28 kD Observed band size: 28 kD Paraformaldehyde-fixed, paraffin embedded (Rat colon); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Antibody incubation with (BRMS1) Polyclonal Antibody, Unconjugated (SL8686R) at 1:400 overnight at 4°C, followed by operating according to SP Kit(Rabbit) (sp-0023) instructionsand DAB staining. Paraformaldehyde-fixed, paraffin embedded (Mouse placenta); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Antibody incubation with (BRMS1) Polyclonal Antibody, Unconjugated (SL8686R) at 1:400 overnight at 4°C, followed by operating according to SP Kit(Rabbit) (sp-0023) instructionsand DAB staining.

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